study of pulmonary function tests in cardiac...
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“STUDY OF PULMONARY FUNCTION TESTS IN CARDIAC
PATIENTS”
Dissertation submitted to
THE TAMIL NADU DR.M.G.R. MEDICAL UNIVERSITY
CHENNAI, TAMIL NADU
in partial fulfillment for the Degree of
DOCTOR OF MEDICINE - BRANCH I GENERAL MEDICINE
APRIL 2016
TIRUNELVELI MEDICAL COLLEGE HOSPITAL
TIRUNELVELI – 11, TAMIL NADU
CERTIFICATE
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This is to certify that the Dissertation entitled “STUDY OF
PULMONARY FUNCTION TESTS IN CARDIAC PATIENTS”submitted by
Dr.M.MATHAN to The TamilnaduDr. M.G.R. Medical University, Chennai, in
partial fulfillment for the award of M.D.Degree(GENERAL MEDICINE) is a
bonafide work carried out by him under my guidance and supervision
during the course of study 2013-2016. This dissertation partially or fully has
not been submitted for any other degree or diploma of this university or
other.
Prof. Dr. M.R.VAIRAMUTHURAJU.
MD Professor and HOD,
Department of Medicine,
Tirunelveli Medical College ,
Tirunelveli – 627011.
Prof.Dr.K.SITHY ATHIYA MUNAVARAH.M.D
The Dean,
Tirunelveli Medical College,
Tirunelveli – 627 011.
Prof.Dr.ARUMUGAPANDIAN S. MOHAN
M.D.,
CHIEF UNIT II, Department of Medicine,
Tirunelveli Medical College, Tirunelveli.
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ACKNOWLEDGEMENT
I would like to thank THE DEAN DR.SITHY ATHIYA
MUNAVARAH M.D,Tirunelveli Medical College,Tirunelveli for
permitting me to utilize the hospital facilities for the dissertation.
I also extend my sincere thanks to Professor Dr.VAIRAMUTHU
RAJU M.D, Head of the Department , Department of General Medicine for
his constant support during the study.
I would like to express my deep sense of gratitude and thanks to
my Unit Chief Professor.Dr.ARUMUGAPANDIAN S. MOHAN M.D, my
guide and Professor of Medicine for his valuable suggestions and excellent
guidance during the study.
I thank the Assistant Professors of my unit Dr. R.PERIYASAMY
M.D, Dr. A.RAJESH M.D and Dr. MARCHWIN KINGSTON M.D for
their help and constructive criticisms.
I offer my special thanks to Dr.KRISHNAMOORTHY M.D,
Head of the Department, Chest Medicine for his kind cooperation and
valuable guidance .
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I thank all the patients who participated in the study for their
extreme patience and kind cooperation .
I wish to acknowledge all those , including my postgraduate
colleagues, my parents who have directly or indirectly helped to complete
this work with great success.
Above all I thank the Lord Almighty for his kindness and
benevolence.
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ABBREVIATIONS
RHD- rheumatic heart disease
CCF-congestive cardiac failure
MI- myocardial infarction
CHF-congestive heart failure
SLE- systemic lupus erythematosis
LVH-left ventricular hypertrophy
LVF- left ventricular failure
IHD- ishemic heart disease
HTN-hypertension
PND-paroxysmal nocturnal dyspnea
BUN-blood urea nitrogen
BNP-brain natriuretic peptide
CHD- congenital heart disease
CAHD-coronary artery heart disease
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PFT-pulmonary function tests
FVC - Forced Vital Capacity
FEV1 - Forced Expiratory Volume in One Second
FEV3 - Forced Expiratory Volume in Three Seconds
PEFR - Peak Expiratory Flow Rate
FEF - Forced Expiratory Flow
MVV - Maximal Voluntary Ventilation
VC- vital capacity
RC- residual capacity
TLC-Total lung capacity
COPD-chronic obstructive pulmonary disease
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CONTENTS
No TITLE PAGE NUMBER
1) INTRODUCTION 10
2) AIM AND OBJECTIVES 13
3) REVIEW OF LITERATURE 15
4) MATERIALS AND METHODS 68
5) OBSERVATIONS 73
6) DISCUSSION 90
7) CONCLUSION 94
8) BIBLIOGRAPHY 96
9) ANNEXURE 99
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INTRODUCTION
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Coronary artery heart disease and rheumatic heart disease are
among the most common causes of morbidity and mortality in India. These two
diseases are the most common causes of cardiac failure. Patients with these
diseases should have regular follow-up with doctors.
Heart failure is seen to be a highly common disease affecting about
1% of people in their 50s and increasing rapidly to 10% prevalence in their
80s.The annual incidence range is from 0.2% in 45 to 55 years of age to
4% in 85 to 95 years of age, with approximate doubling in each decade of
life. Male predominance is seen because of high incidence of coronary
artery heart disease occurring in males which in turn leads to 4 times
increased risk of heart failure.
Impaired pulmonary function is common in cardiac patients.
Respiratory muscle wasting has been well documented in Rheumatic Heart
Disease patients. But Pulmonary Function Test is the least common test that
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is undergone by the patients. This current study is aimed to assess the
Pulmonary Function of cardiac patients with coronary artery heart disease
and rheumatic heart disease who have recovered from cardiac failure.
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AIM AND OBJECTIVES
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To study the Pulmonary Function Test patterns in patients with coronary
artery heart disease and Rheumatic Heart Disease who have revived from
Cardiac Failure.
To diagnose any underlying undiagnosed respiratory problem coexisting
with cardiac failure.
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REVIEW OF LITERATURE
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CARDIAC FAILURE
Cardiac failure is nowadays one of the common cause for
IMCU admissions in any hospital. It is defined as the inability of the heart to
pump sufficiently to maintain blood flow to meet the body‟s needs. There
are numerous causes that lead on to cardiac failure such as Hypertension,
Coronary Artery Heart Disease, Vavular Heart disease, Cardiomyopathy,
Anemia, etc.
Many disease processes can impair the pumping efficiency
of heart leading on to congestive heart failure[7]
.Heart failure means the
inability of the heart to adequately meet the needs of organs and tissues for
oxygen and nutrients. This decrease in cardiac output is not enough to
circulate the blood returning to the heart from the body and lungs leading to
fluid leak from capillary blood vessels. This leads to the symptoms like
breathing difficulty, weakness and swelling.
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BLOOD CIRCULATION IN THE BODY:-
The right side of heart pumps blood to lungs for
oxygenation[5]
while left side pumps blood to rest of the body. Deoxygenated
blood from the body enters the right atrium through superior and inferior
vena cavae. Then it flows in to the right ventricle through tricuspid valve
from where it is pumped into the lungs through the pulmonary artery. In the
lungs it gets oxygenated, returns to the left atrium via 4 pulmonary veins
.Then it enters left ventricle and distributed to the organs and tissues of the
body[2]
through aorta and its branches.
Oxygen enters RBCs, while Carbon-di-oxide an excretory product of
metabolism is removed in the lungs. The cycle then repeats.
Left heart failure results when left ventricle is not able to pump blood to the
body and fluid gets back logged, leaks in to the lungs causing
breathlessness.Right heart failure occurs when right ventricle is not able to
pump blood from the body in to the lungs for oxygenation. Blood and fluid
gets back logged in the venous system, leading on to fluid leak into tissues
and organs.
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Both sides of the heart may fail at the same time leading on to biventricular
heart failure.
Many disease entities can damage the pumping capacity of
the heart leading on to CCF.
The most common causes for CCF are[6]
Coronary Artery Heart Disease
Hypertension
Chronic Alcoholism
Valvular Heart Disease
Toxic /Metabolic Diseases
Myocarditis
Congenital Heart Disease
Arrhythmias
Cardiomyopathy.
Less common causes are
Viral infections of heart muscle
Hypothyroidism and hyperthyroidism
Drug induced (NSAIDS , steroids, Pioglitazone, CCB)
Amyloidosis
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Emphysema
Severe Anemia
Iron overload
Sarcoidosis
Causes of refractory cardiac failure
Silent MI
Pulmonary emboli
Thyrotoxicosis
LV aneurysm
Silent valvular stenosis
BeriBeri
Anemia
Myocarditis
Infection
Infective endocarditis
Cardiac tamponade
SA / AV nodal dysfunction
RISK FACTORS OF CHF[4]
It often results from atherosclerotic heart disease and hence the risk factors
are the same.
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Uncontrolled hypertension
Increased blood cholesterol
Diabetes
Smoking
Family history
Obstructive sleep apnoea
Alcohol
Drug abuse
Connective tissue disorders like SLE
Many patients will have a stable CHF that can decompensate on bodily
changes. Suppose a patient with compensated CHF may be doing well but when
something like respiratory infections or angina develops, it may precipitate heart
failure. A decompensatory state may develop acutely when patient takes excessive
liquid or salt or not taking his routine prescribed drugs.
PATHOPHYSIOLOGY
Low cardiac output leads to decreased perfusion and inadequate oxygen
supply along with assosiated decreased cardiac reserve, pulmonary and systemic
venous compliance.
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Compensatory adaptation:-
1.Increase in left ventricular mass (LVH) and volume (dilatation)
2. Increased systemic vascular resistance
3.Activation of renin – angiotensin – aldosterone and vasopressin (ADH)
system.
PRELOAD
Preload is the left ventricular end diastolic pressure and it depends on left
ventricular compliance and venous return.
AFTERLOAD:-
Afterload is the left ventricular systolic wall tension that develops during
ventricular systole and is determined by aortic valve resistance , peripheral
vascular resistance and elasticity of major blood vessels.
CLASSIFICATION OF CARDIAC FAILURE
HIGH OUTPUT AND LOW OUTPUT FAILURE[2]
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1.HIGH OUTPUT FAILURE
The heart is normal and it fails to maintain a normal or increased
output during greatly increased demand situations like anemia,
hyperthyroidism , Paget‟s disease ,A-V malformation , pregnancy. First,
features of RVF appear , later LVF features become evident. The only clue
to the development of LVF in patients with high output states is presence of
shortened circulatory time.
2.LOW OUTPUT FAILURE
The heart fails to generate adequate output or can do so with high filling
pressures.
The causes of low output failure are
i)Intrinsic heart muscle disease (Cardiomyopathy, IHD, Myocarditis, Chagas
disease)
ii)Chronic excessive after load (Aortic stenosis , HTN)
iii)Chronic excessive preload (Mitral Regurgitation)
iv)Negative inotropic drugs (Anti arrhythmic agents)
v)Restricted filling (eg. Constrictive pericarditis or tamponade , restrictive
cardiomyopathy)
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vi)Extreme bradycardia (beta blockers , complete heart block)
RIGHT AND LEFT SIDED HEART FAILURE
1. RIGHT SIDED HEART FAILURE
Right sided heart failure is characterised by peripheral edema,
abdominal discomfort (congestive hepatomegaly), raised JVP and
hypotension. Usually there is no evidence of pulmonary edema.
2. LEFT SIDED HEART FAILURE
The classical feature of LVF is presence of pulmonary edema. Other
signs are tachypnoea , tachycardia ,S3 ,pulsus alternans & cardiomegaly.
3.CONGESTIVE HEART FAILURE
Congestive heart failure has both the features of right and left sided
heart failure.
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FORWARD AND BACKWARD HEART FAILURE
1.FORWARD HEART FAILURE
Inadequate pumping of blood into the arterial system leads to
poor tissue perfusion. Poor renal perfusion results in excessive sodium
reabsorption through activation of Renin –Angiotensin-Aldosterone system.
2.BACKWARD HEART FAILURE
Due to the failure of one or the other ventricle to fill normally
and discharge its contents, causing an elevated arterial and venous system
pressure behind the failing ventricle.
SYSTOLIC AND DIASTOLIC FAILURE
1.SYSTOLIC FAILURE
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Systolic failure occurs when there is inadequate cardiac output and
usually associated with cardiomegaly. Patients with systolic failure are
usually treated with ionotropic agents.
2.DIASTOLIC FAILURE
Diastolic failure is associated with increased resistance to
ventricular inflow and reduced ventricular diastolic capacity. The patients
are usually managed with vasodilator therapy.
NYHA (New York Heart Association) FUNCTIONAL
CLASSIFICATION OF HEART FAILURE
CLASS FUNCTIONAL CAPACITY
I Patient without limitation of physical activity
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II Patient with slight limitation of physical capacity in which
ordinary physical activity leads to fatigue, palpitation,
dyspnoea or angina.
III Patient with marked limitation of physical capacity in which,
less than ordinary physical activity leads to symptoms of
heart failure.
IV Symptoms of heart failure even at rest.
CLINICAL FEATURES:-
Signs and symptoms include
Dyspnoea on exertion or dyspnoea at rest
Orthopnoea (while lying flat)
Paroxysmal nocturnal dyspnoea (May awaken person from sleep)
Acute pulmonary edema
Chest pain and palpitation
Tachycardia
Fatigue and weakness
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Nocturia and oliguria
Anorexia , weight loss
Exophthalmos or visible pulsation of eye
Neck vein distension
Weak ,rapid and threading pulse
Rales , wheeze
S3 gallop +/- , pulsus alternans
Increased intensity of second heart sound
Hepato jugular reflex
Ascites ,hepatomegaly , anasarca
Cyanosis (central and peripheral) Pallor
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DIAGNOSIS:-
1. RELEVANT HISTORY
2. PROPER PHYSICAL EXAMINATION
3. INVESTIGATIONS
i) ECG
ECG helps to assess the heart rate, rhythm and indirectly the size of
ventricles and blood flow to heart muscle.
ii) CHEST X-RAY
To look for heart size and presence or absence of fluid in the lungs
Prominent upper lobe veins- pulmonary capillary wedge pressure >15mmHg
Kerley B lines (engorged peripheral lymphatics seen in lower lobe PCWP
>20mmHg
Fluid in the fissures or interlobar effusion known as „phantom tumour‟ as it
disappears with treatment of left sided failure.
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Increase in bronchovascular markings, Chat‟s wing or inverted moustache
signs- PCWP >25mmHg
Pleural effusion – may be unilateral or bilateral
Cardiomegaly
iii) BLOOD TESTS
CBC, electrolytes, glucose, BUN and creatinine (to assess kidney function)
iv) B TYPE NATRIURETIC PEPTIDE
This hormone is produced by right and left ventricular muscle cells and released in
response to stretch, volume overload and elevated filling pressures. It is very
specific and sensitive. It identifies or excludes heart failure. It is extremely useful
in diagnosis, prognosis and monitoring the therapy. Serum levels of BNP is
increased in heart failure and also in asymptomatic LV dysfunction. BNP level
< 100pg/ml excludes cardiac failure.
Uric acid, CRP, trop I andT, TNF receptors are other biomarkers of heart failure.
v) ECHOCARDIOGRAPHY
To assess the anatomy and function of the heart. It can assess blood flow of the
heart, chamber enlargement, contractility and measures ejection fraction.
vi) ANGIOGRAPHY
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4. FRAMINGHAM CRITERIA FOR DIAGNOSIS OF
CCF
MAJOR CRITERIA:-
PND
Neck vein engorgement
Crackles-lung field
Cardiomegaly
Acute pulmonary edema
S3 gallop
Increase venous pressure (>16cm H2O)
Positive hepato jugular reflex
MINOR CRITERIA
Extremity edema
Nocturnal cough
Dyspnoea on exertion
Pleural effusion
Tachycardia (120 bpm)
Decreased vital capacity by 1/3
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MAJOR/ MINOR CRITERIA
5 days treatment causing weight loss > or equal to 4.5 kg
FOR DIAGNOSIS: 1 MAJOR +2 MINOR
TREATMENT OF CARDIAC FAILURE:-
GENERAL PRINCIPLES OF MANAGEMENT:-
1. Removal of precipitating causes:-
Like anemia, arrhythmia, pregnancy, infection, thyroid disorders,smoking and
alcohol ,drugs, hypertension, MI, pulmonary embolism ,dietary and medical non
compliance.
2. Correction of underlying causes like CHD, RHD.
3. Control of fluid and sodium retention.
4. Enhancement of myocardial contractility.
5. Reduction of pulmonary and systemic venous congestion.
6. Minimisation of cardiac work load.
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In this study we are dealing with coronary artery heart
disease and rheumatic heart disease patients who were recovered from
cardiac failure. Hence we discuss a few points from coronary artery heart
disease and rheumatic heart disease.
CORONARY ARTERY HEART DISEASE:-
Coronary artery heart disease is one of the important causes
for cardiac failure. It comprises a group of diseases which vary from stable
angina, unstable angina, myocardial infarction to sudden cardiac death.
One third of all deaths globally were due to coronary artery
heart disease. Nearly 7.6 million deaths annually are attributed to coronary
artery heart disease. By 2030 researchers project that CAHD alone will be
the cause of more deaths than infectious diseases in developing and under
developed countries.
Chest pain is the most common symptom of CAHD which is
compressive in nature felt retrosternally radiating to shoulder, arm, jaw, and
epigastric region getting aggravated on exertion relieved by taking rest or
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nitrates. Other symptoms include fatigue, breathlessness, syncope and
palpitation.
Risk factors for CAHD are
1. Hypertension
2. Diabetes mellitus
3. Smoking
4. Alcohol
5. Sedentary life style
6. Obesity
7. Hyperlipidemia
8. Depression
PATHOPHYSIOLOGY:-
Decreased blood flow to the cardiac muscle fibres causes ischemia of
the myocardial cells. These cardiac cells may die due to lack of oxygen and
this is called myocardial infarction which leads to heart muscle death ,
myocardial scarring without heart muscle regrowth. Atherosclerosis when
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develops within the smooth elastic lining inside the coronary artery leads to
CAHD. Due to the same, the inner wall of the artery hardens, stiffens and
swollen with calcium deposits, fatty deposits, certain inflammatory cells to
form the plaque. Rupture of these plaques cause contact between
coagulation factors of blood and thrombogenic tissue factor which is
expressed by macrophage foam cells. If a thrombus formed due to this
mechanism is non occlusive, an episode of plaque disruption sometimes
does not cause symptoms or otherwise causes episodic ischemic features.
Occlusive thrombi in the absence of collaterals supplying coronary artery
causes acute myocardial infarction.
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DIAGNOSIS:-
CAHD can be diagnosed using following investigations
1.Electrocardiogram(ECG)
2.Echocardiogram
3.Cardiac enzymes
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4.Stress test
5.Cardiac catheterization or Angiogram
6.Heart scan
7.Magnetic resonance angiogram
TREATMENT:-
Treatment for CAHD include
1.PCI
2.Antifibrinolytics such as streptokinase and urokinase
3. Injection Heparin
4.T.Aspirin
5.T.Clopidogrel
6.T.Atorvastatin
7.T.Sorbitrate
8.ACE inhibitors like T. Enalapril, T.Ramipril etc.
9.Beta blockers like T.Carvedilol , T.Bisoprolol and T.Metaprolol
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RHEUMATIC HEART DISEASE
RHD which is the most common cause of heart disease in
children globally, results in permanent damage to the heart specifically
heart valves following rheumatic fever .The most common valves affected
in RHD are mitral valve and aortic valve . Despite its declining trend it still
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causes a heavy burden in the social and economic life in developing
countries.
Acute rheumatic fever is a post infectious sequelae of pharyngitis caused by
group A beta hemolytic streptococci . Risk factors of rheumatic fever
includes overcrowding , poor sanitation and other conditions causing
multiple exposure to streptococcus bacteria.
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CLINICAL FEATURES:-
Clinical features of rheumatic fever may vary which includes
1. Fever
2. Migrating painful joints
3. Red hot inflamed joints
4. Small painless subcutaneous nodules
5. Chest pain
6. Painless ragged raised rash
7. Uncontrollable semi purposeful abnormal movements
8. Unusual behavior such as inappropriate laughter and crying
DIAGNOSIS
Diagnosis of rheumatic fever is based on revised Jones criteria, which
says two major or one major and two minor criteria associated with
evidence of group A streptococcal infection can be diagnosed as rheumatic
fever.
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MAJOR CRITERIA
1. Pancarditis
2. Migrating polyarthritis involving major joints
3. rheumatic chorea ( syndenham‟s)
4. Erythema marginatum
5. Subcutaneous nodules
MINOR CRITERIA
1. Fever
2. Polyarthralgia
3. Elevated ESR and leucocyte count
4. Prolonged PR interval in ECG
5. elevated CRP
SUPPORTING EVIDENCE
1. Elevated anti streptolysin O titre
2. Positive throat culture
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3. Rapid antigen test for group A streptococcus
4. Recent scarlet fever
TREATMENT:-
The treatment for acute rheumatic fever includes Injection Crystalline
Penicillin 1.0 million units i.v 4-6th
hourly for 1 week or tablet Penicillin
500 mg (250 mg for children) per oral twice daily with tablet Aspirin 80 to
100 mg/ kg per day for two weeks. The use of glucocorticoids in acute
rheumatic fever remains controversial.
PROPHYLAXIS:-
Prophylaxis is given by injection Benzathine Penicillin 1.2 million
units deep im (6 lakh units if less than 27 kg ) under the following schedule.
1.Without carditis –5 years following last attack or age 21 whichever is
longer
2.With carditis but no residual valvular lesion- 10 years following last
attack or age 21 whichever is longer.
3.Persistent valvular lesion- lifelong .
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LUNG FUNCTION TESTS
Lung function tests[9]
measure how lungs take in air and exhale and
also how efficiently they transfer oxygen into the blood. There are a lot of
tests included in Pulmonary function tests.It is a generic term used to
indicate a battery of studies or manoeuvres that may be performed using
standardized equipment to measure lung function.
It evaluates one or more aspects of the respiratory system
– Respiratory mechanics
– Lung parenchymal function/ Gas exchange
– Cardiopulmonary interaction
Pulmonary function tests can be classified broadly into
MECHANICAL/ VENTILATORY FUNCTIONS OF LUNG / CHEST WALL
BED SIDE PULMONARY FUNCTION TESTS
STATIC LUNG VOLUMES & CAPACITIES – VC, IC, IRV, ERV,
RV,FRC.
DYNAMIC LUNG VOLUMES –FVC, FEV1, FEF 25‐75%,
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PEFR, MVV, RESP. MUSCLE STRENGTH
GAS‐ EXCHANGE TESTS
ALVEOLAR‐ARTERIAL PO2 GRADIENT
DIFFUSION CAPACITY
GAS DISTRIBUTION TESTS‐
1) SINGLE BREATH N2 TEST.
2) MULTIPLE BREATH N2 TEST
3) HELIUM DILUTION METHOD
4) RADIO Xenon SCINITIGRAM
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SPIROMETRY: CORNERSTONE OF ALL PFTs.
John hutchinson – invented spirometer.
“Spirometry is a medical test that measures the volume of air an individual
inhales or exhales as a function of time.”
CAN‟T MEASURE – FRC, RV, TLC
The main gadget used in pulmonary function testing is the
spirometer. It is designed to measure changes in volume and can only
measure lung volume in chambers that exchanges gas with the atmosphere.
Spirometers with electronic signal outputs (pneumotachs) also measure flow
(volume per unit of time). A device is usually always attached to the
spirometer which measures the movement of gas in and out of the chest and
is referred to as a spirograph. Sometimes the spirograph is replaced by a
printer like unit. The resulting tracing is called a spirogram. Many
computerized systems have complex spirographs or printouts that show the
predicted values next to the observed values (the values actually measured).
The unit will have in memory all of the prediction tables for males and
females across all age groups. In special spirometers, there are special tables
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of normal values programmed into the machine for selection when Blacks,
children or other groups are being tested who may vary from the normal PFT
tables established for caucasian adults.
There are a few variables such as age, gender and body size which may have an
impact on the lung function of one individual compared to another.
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INDICATIONS FOR SPIROMETRY[12]
1.DETECTING PULMONARY DISEASE
History of pulmonary symptoms
Chest pain or orthopnea
Cough or phlegm production
Dyspnea or wheezing
Physical findings
Chest wall deformities
Cyanosis
Decreased respiratory sounds
Finger clubbing
Abnormal laboratory findings
Abnormal blood gas analysis
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Abnormal Chest xray
2.ASSESSING SEVERITY OR PROGRESSION OF DISEASE
Pulmonary diseases
Chronic obstructive pulmonary disease
Cystic fibrosis
Interstitial lung diseases
Sarcoidosis
Cardiac diseases
Congestive heart failure
Congenital heart disease
Pulmonary hypertension
Neuromuscular diseases
Amyotrophic lateral sclerosis
Guillain-Barré syndrome
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Multiple sclerosis
Myasthenia gravis
3.RISK STRATIFICATION OF PATIENTS FOR SURGERY
Thoracic surgeries
Lobectomy
Pneumonectomy
Cardiac surgeries
Coronary bypass
Correction of congenital abnormalities
Valvular surgery
Organ transplantation
General surgical procedures
Cholecystectomy
Gastric bypass
4. EVALUATING DISABILITY OR IMPAIRMENT
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Social Security or other compensation programs
Legal or insurance evaluations
CONTRAINDICATIONS OF SPIROMETRY
Acute disorders affecting test performance (e.g.,vomiting, nausea, vertigo)
Hemoptysis of unknown origin (FVC maneuver may aggravate underlying
condition.)
Pneumothorax
Recent abdominal or thoracic surgery
Recent eye surgery (increases in intraocular pressure during spirometry)
Recent myocardial infarction or unstable angina
Thoracic aneurysms (risk of rupture because of increased thoracic pressure)
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FACTORS AFFECTING SPIROMETRY VALUES[10]
Age:
The natural elasticity of the lungs decreases with age. As age
increases lung volumes and capacities become smaller and smaller. So it is
important to compare the results of a normal person of the same age and
gender while interpreting spirometry values.
Gender:
Usually males have more lung volumes and capacities compared to
females even when they are matched for height and weight. Because of this
difference in lung volumes and capacities, different normal tables must be
used for males and females.
Body Height &Size:
Body size has huge effects on PFT values.The PFT result of a small
man will be smaller than a man of the same age who is much larger. Normal
tables give predicted PFT data for males or females of a certain age and
height by accounting for this variable .As people age they begin to increase
their body mass by increasing their body fat to lean body mass ratio. The
abdominal mass prevents the diaphragm from descending as far as it could
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and the PFT results will be below the expected PFT values - i.e. the
observed (measured)values are actually smaller than the predicted values
(predicted values from the normal tables) if they become too obese.
Race:
The PFT values are affected by race also. Blacks, Hispanics and
Native Americans have different PFT results compared to Caucasians.
Hence while interpreting PFT values of a patient , we should use a race
appropriate table to compare the patient's measured pulmonary function
against the results of the normal table written for that patient's racial group.
The degree of effect on PFT is not clearly understood for other
factors such as environmental factors and altitude but may have effect on
PFT.
PREPARING THE PATIENT
The patientsshould be comfortable and they should be seated since
there is a chance of faintness or syncope during the procedure. Before doing
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the test the purpose of the test should be explained to the patient .Ideally the
correct technique is demonstrated before asking the patient to use a
spirometer for the first time. And ask the patient to have some practice
sessions before the readings are taken. Encourage the patient to keep
blowing out so that maximal exhalation can be achieved. The total number
of times the patient takes for practice and recording is limited to eight or
less at each session.
SPIROMETRIC VALUES
Lung function is physiologically divided into four volumes: expiratory
reserve volume, inspiratory reserve volume, residual volume, and tidal
volume. The sum of all these four volumes make the total lung capacity
(TLC). Lung volumes and their combinations measure various lung
capacities such as functional residual capacity(FRC), inspiratory capacity,
and VC.[11]
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FVC - Forced Vital Capacity :-
This is the volume of air which can be forcibly and maximally
exhaled out of the lungs after a deep inspiration . FVC is usually expressed
in units called liters. This PFT value is very significant in the diagnosis of
obstructive and restrictive diseases.
FEV1 - Forced Expiratory Volume in One Second
This is the amount of air which can be forcibly exhaled from the lungs
in the first second of a forced expiratory manoeuvre. It is expressed as litres
This PFT value is very significant in the diagnosis of obstructive and
restrictive diseases.
FEV1/FVC - FEV1 Percent (FEV1%)
This measurement is the ratio of FEV1 to FVC - it indicates what
percentage of the total FVC was expelled from the lungs during the first
second of forced exhalation - this number is called FEV1%, %FEV1 or
FEV1/FVC ratio. This value helps in the diagnosis of obstructive and
restrictive diseases.
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FEV3 - Forced Expiratory Volume in Three Seconds
This is the volume of air which can be forcibly exhaled in three
seconds - measured in Litres - this volume usually is almost close to the
FVC, since in the normal individual most of the air in the lungs can be
forcibly exhaled in three seconds.
FEV3/FVC - FEV3%
This number is the ratio of FEV3 to the FVC - it indicates what
percentage of the total FVC was expelled during the first three seconds of
forced exhalation. This is called %FEV3 or FEV3%.
PEFR - Peak Expiratory Flow Rate
This is maximum flow rate achieved by the patient during the forced
vital capacity manoeuvre beginning after full inspiration and starting and
ending with maximal expiration - it can either be measured in L/sec or L/min
- this is a useful measure to see if the treatment is improving obstructive
diseases like bronchoconstriction due to asthma.
FEF - Forced Expiratory Flow
Forced expiratory Flow is a measure of how much air can be expired
from the lungs. It is a flow rate measurement. It is measured as liters/second
60
or liters/minute. The FVC expiratory curve is divided into quartiles and
therefore there is a FEF that existsfor each quartile. The quartiles are
expressed as FEF25%, FEF50%, and FEF75% of FVC.
FEF25%
This measurement describes the amount of air that was forcibly
expelled in the first 25% of the total forced vital capacity test.
FEF50%
This measurement describes the amount of air expelled from the lungs
during the first half (50%) of the forced vital capacity test. This test is useful
when looking for obstructive disease.The amount of air that will have been
expired in an obstructed patient is smaller than that measured in a normal
patient.
FEF25%-75%
This measurement describes the amount of air expelled from the
lungs during the middle half of the forced vital capacity test. Many
physicians like to look at this value because it is an indicator of obstructive
disease.
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MVV - Maximal Voluntary Ventilation: -
This value is determined by having the patient breathe in and out as
rapidly and fully as possible for 12 -15 seconds - the total volume of air
moved during the test. Usually expressed as L/sec or L/min . The value helps
to assess the status of the respiratory muscles, compliance of the thorax-lung
complex, and airway resistance. Drawback of the test is that it is effort
dependant and therefore can be a poor predictor of true pulmonary strength
and compliance.
MEASURMENT OF FEV1 AND FVC
To measure the values first attach a disposable, clean, one-way
mouthpiece to the spirometer (a fresh one for each patient) and the patient is
asked to breathe in as deeply as possible (full inspiration).
The patient should hold their breath just long enough to seal their lips.
The patient should NOT purse their lips as if blowing a trumpet, and ideally
should pinch their nose or wear a nose clip. The patient should now blow the
breath out, forcibly, as hard and as fast as possible, until there is nothing left
to expel.
62
Patient should be encouraged to keep blowing out. Some spirometers
give a beep to confirm the manoeuvre is complete. Now repeat the procedure
two times.
Ideally three readings should be obtained of which the best two
which are within 100ml, or 5%, of each other. Depending on model of
spirometer the results may be displayed or directly printed into a strip.
63
Spirometry indicates the presence of an abnormality if any of the following
are recorded:
• FEV1 <80% predicted normal
• FVC <80% predicted normal
• FEV1/FVC ratio <0.7
Obstructive disorder:
• FEV1 decreased (<80% predicted normal)
• FVC is usually found to be reduced but to a smaller extent than FEV1
• FEV1/FVC ratio decreased (<0.7)
Restrictive disorder:
• FEV1 decreased(<80% predicted normal)
• FVC decreased (<80% predicted normal)
• FEV1/FVC ratio normal (>0.7)
64
MEASURING VITAL CAPACITY (VC)
The VC is a non-forced manoeuvre and usually greater than the FVC
in COPD. It shows more accurate measurement of lung volume when
airways are floppy, as in emphysema. It is usually calculated at the
beginning of the procedure to understand the patient with the equipment.
• a fresh ,new, clean, disposable, one-way mouthpiece is attatched to the
spirometer
• patient should breathe in as deeply as possible (in full inspiration).
• Patient is asked to hold their breath just long enough to seal their lips. The
patient should NOT purse their lips as if blowing a trumpet, and ideally
should pinch their nose or wear a nose clip.
• Breathe out steadily, slowly at a comfortable pace.
• Continue until expiration is complete.
• The measurement of slow VC may allow the assessment of airflow
obstruction in patients who are unable to perform a forced measurement to
full exhalation.
65
FLOW-VOLUME MEASUREMENT
Spirometers can measure expiratory flow plotted against the volume of air
exhaled. The graph produced is called a flow-volume curve. The overall shape
of the flow-volume curve is helpful for detecting airflow obstruction at an early
stage, and yields additional information to the volume-time curve. However,
interpretation of the flow-volume curve must take into account the values of
FEV1 and FVC (as a % of predicted normal).
66
Normal flow-volume curves
On exhalation, there is a fast rise to the maximal expiratory flow
continued by a steady, uniform decrease until all the air is exhaled.
Obstructive disorder:
In a patient with obstructive airways disease, the peak expiratory flow
(PEF) is decreased and the decline in airflow to complete exhalation follows
a distinctive dipping (or concave) curve.
Severe obstructive disorder:
In a severe airflow obstruction, especially with emphysema, the
characteristic „steeple pattern‟ is seen in the expiratory flow graph.
Restrictive disorder:
The graph observed in the expiratory trace of a patient with restrictive
defect is normal in shape but there is an absolute reduction in volume.
There are many studies done globally in assessing the pulmonary
function test in cardiac patients .Certain studies indicated impaired
pulmonary function is common in cardiac patients but more deterioration
67
was found as a complication following coronary artery bye pass graft
surgery rather than CAHD and RHD . Respiratory muscle weakness was
documented in various studies in rheumatic valvular heart disease such as
mitral stenosis .
68
MATERIALS AND METHODS
This study is a observational study conducted in Department of
Medicine, Tirunelveli Medical College Hospital. Seventy five patients
admitted in TVMCH from MAY 2014 to MAY 2015 will participate in the
study. The volunteer patients who met the inclusion criteria, signed a
consent form after they got a clear explanation of the spirometry evaluation
procedures.
Inclusion Criteria :
Adult patients with Rheumatic Heart Disease (Male and Female)
Coronary artery heart disease patients less than 60 years of age (Male and
Female)
Exclusion Criteria :
Pediatric patients less than 12 years of age and Adult patients more than 60
years of age
Rheumatic Heart disease patients with known respiratory disease (COPD,
BronchialAsthma, Pulmonary Tuberculosis)
CAHD patients with known respiratory disease(COPD,
BronchialAsthma,Pulmonary Tuberculosis)
Morbid and sick patients
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Severe Left Ventricular Dysfunction patients as per ECHO report.
DATA COLLECTION
Detailed medical history and physical examination will be done
Basic Laboratory investigations such as complete blood count , RFT and
Urine analysis done
ECG
X-Ray Chest PA view
Echocardiogram
Spirometry test
SPIROMETER
The spirometry is performed using a device called a spirometer,which
comes in several different varieties. Most spirometers display the following
graphs,calledspirograms:
A volume-time curve, showing volume (liters)along the Y-axis and time
(seconds) along the X-axis
A flow-volume loop,which graphically depicts the rate of airflow on the Y-
axis and the total volume inspired or expired on the X-axis
70
PROCEDURE
The basic forced volume vital capacity (FVC) test varies slighty
depending on the equipment used.
Generally, the patient is asked to take the deepest breath they can, and
then exhale into the sensors hard as possible, for as long as possible,
preferably at least 6 seconds. It is sometimes directly followed by a rapid
inhalation(inspiration),in particular when assessing possible upper airway
obstruction. Sometimes, the test will be preceded by a period of quiet
breathing in and out from the sensor (tidal volume) or the rapid breath in
(forced inspiratory part ) will come before the forced exhalation.
During the test, soft nose clips may be used to prevent air escaping
through the nose. Filter mouthpieces may be used to prevent the spread of
microorganisms.
71
LIMITATIONS OF TEST
The manoeuvre is highly dependent on patient cooperation and effort,
and is normally repeated at least three times to ensure reproducibility. Since
results are dependent on patient cooperation, FVC can only be
underestimated, never overestimated.
Due to the requirement of patient cooperation , spirometry can only
be used on children old enough to comprehend and follow the instructions
given(6 years old or more),and only on patient who are able to understand
and follow instructions- thus, this test is not suitable for patients who are
unconscious ,heavily sedated ,or have limitations that would interfere with
vigorous respiratory efforts. Other types of lung function tests are available
for infants and unconscious persons.
Another major limitation is the fact that many intermittent or mild
asthmatics have normal spirometry between acute exacerbation, limiting
spirometry‟s usefulness as a diagnostic tool. It is more useful as a
72
monitoring tool. A sudden decrease in FEV1 or other spirometric measure in
the same patient can signal worsening,even if the raw value is still normal.
Patients are encouraged to record their personal best measures .
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OBSERVATIONS AND RESULTS
74
0
5
10
15
20
25
30
35
40
45
50
RHD CAHD
Number of patients
Number of patients
75
MALE FEMALE TOTAL
CAHD 28 18 46
RHD 21 8 29
TOTAL 49 26 75
Among the 75 patients under study, 49 were male and 28 were female
patients. Out of 49 male patients, 28 were having CAHD and 21 were
suffering from rheumatic heart disease. Among the 26 females, 18 were
found to have CAHD and 8 were suffering from rheumatic heart disease.
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STUDY POPULATION
Normal
Obstructive
Restrictive
77
MALE FEMALE TOTAL
NORMAL 26 13 39
OBSTRUCTIVE 8 4 12
RESTRICTIVE 15 9 24
TOTAL 49 26 75
Among 49 males in study population 26 were found to have normal
pulmonary function test parameters, 15 showed restrictive pattern and 8
showed obstructive pattern. Out of 26 females 13 were found to have normal
pattern , 9 showed restrictive pattern and 4 were found to have obstructive
pattern. Among total 75 pateints, 39 patients showed normal pft pattern,24
showed restrictive pattern in pft and 12 were found to have obstructive
pattern.
78
CAHD PATIENTS IN STUDY POPULATION
Normal
Obstructive
Restrictive
79
46 patients among the study population were CAHD patients. Among
them 28 were males and 18 were females. Among 28 males, 18 were having
normal PFT pattern, 5 showed obstructive pattern and 5 showed restrictive
pattern. Among 18 females, 10 showed normal pattern ,3 showed obstructive
pattern and 5 showed restrictive pattern.
MALE FEMALE TOTAL
NORMAL 18 10 28
OBSTRUCTIVE 5 3 8
RESTRICTIVE 5 5 10
TOTAL 28 18 46
80
RHD PATIENTS IN STUDY POPULATION
Normal
Obstructive
Restrictive
81
MALE FEMALE TOTAL
NORMAL 8 3 11
OBSTRUCTIVE 2 1 3
RESTRICTIVE 11 4 15
TOTAL 21 8 29
Among the study population 29 patients were having rheumatic heart
disease. 21 were males and 8 were females. Among the 21 males, 8 showed
normal PFT pattern,3 showed obstructive pattern and 11 were found to have
restrictive pattern. Among the females , 3 were found to have normal
pattern, obstructive pattern in 1 patient and restrictive pattern seen in 4
patients .
82
0 5 10 15 20 25 30
Normal
Obstructive
Restrictive
No. of hypertensive patients
No. of hypertensive patients
83
MALE FEMALE TOTAL
NORMAL 17 11 28
OBSTRUCTIVE 4 1 5
RESTRICTIVE 8 5 13
TOTAL 29 17 46
Among the study population, 46 were found to be hypertensive.
Among them, 29 were males and 17 were females. Among 29 males, 17
were found to have normal PFT pattern, 4 were having obstructive pattern
and 8 were having restrictive pattern. Out of 17 females 11 were having
normal PFT pattern, 5 were having obstructive pattern and 13 showed
restrictive pattern.
84
0 2 4 6 8 10
Normal
Obstructive
Restrictuve
No. of patients with cardiomegaly
No. of patients with cardiomegaly
85
MALE FEMALE TOTAL
NORMAL 5 4 9
OBSTRUCTIVE 2 2 4
RESTRICTIVE 3 4 7
TOTAL 10 10 20
Among the study population , 20 were diagnosed to have
cardiomegaly on chest radiography. Among the 10 males, 5 were having
normal PFT values, 2 showed obstructive pattern and 3 showed restrictive
pattern.among females, 9 were found to have normal PFT study, 4 patients
were having obstructive pattern and 7 showed restrictive pattern.
86
STUDY PATIENTS WITH EF > 50%
NORMAL
OBSTRUCTIVE
RESTRICTIVE
87
MALE FEMALE TOTAL
NORMAL 16 6 22
OBSTRUCTIVE 1 1 2
RESTRICTIVE 9 6 15
TOTAL 26 13 39
Among the study sample, 39 patients were having ejection fraction
more than 50%. Among them 26 were male patients and 13 were female
patients. Among the 26 males, 16 showed normal PFT payyerns,1 showed
obstructive pattern and 9 were showing restrictive pattern. Among
females,normal pattern was seen in 6 patients, obstructive pattern in 1 and
restrictive pattern in 6 patients.
88
STUDY POPULATION WITH EF < 50%
NORMAL
OBSTRUCTIVE
RESTRICTIVE
89
MALE FEMALE TOTAL
NORMAL 10 7 17
OBSTRUCTIVE 6 3 9
RESTRICTIVE 7 3 10
TOTAL 23 13 36
Among the study population 36 patients were having ejection
fraction less than50%. Out of these 36 patients,23 were males and 13 were
females. Among the 23 males 10 were having normal PFT patterns, 6
showed obstructive pattern and 7 showed restrictive pattern. Out of 13
females, 7 were having normal PFT pattern, obstructive pattern seen in3
patients and restrictive pattern in 3 patients.
90
DISCUSSION
91
Heart failure is one of the common causes of mortality and morbidity
of Indian population. However the pulmonary function of such patients has
not been studied adequately. This study, “STUDY OF PULMONARY
FUNCTION TESTS IN CARDIAC PATIENTS “is a observational study
done on 75 patients with cardiac failure admitted in Tirunelveli medical
college hospital, after they were revived from cardiac failure.
A study population included 49 male patients and 26 female patients.
Of the male patients 29 were diagnosed to be having coronary artery heart
disease and 20 patients were diagnosed to be having Rheumatic Heart
Disease. Among the 26 female patients 17 were found to be having coronary
artery heart disease and 9 were found to be having Rheumatic Heart Disease.
In this study pulmonary function test was done on these patients once
they revived from cardiac failure. The parameters studied were forced
expiratory volume in first second (FEV1), forced vital capacity (FVC), and
ratio of FEV1/FVC. From these parameters whether these patients were
having obstructive or restrictive pattern of respiratory involvement was
studied. Supportive investigations such as chest x-ray PA view, ECG and
Echocardiogram was done.
92
Among the studied patients 52% had normal pattern of pulmonary
function test, 32% had restrictive pattern and 16% had obstructive pattern.
Out of the male patients 53.06% had normal pattern, 30.61% had restrictive
pattern and 16.32% had obstructive pattern. Out of the female patients
studied, 50% had normal pattern, 34.61% had restrictive pattern and 15.38%
had obstructive pattern. This shows that both males and females in the study
population had similar type of distribution of the pulmonary function test
pattern.
61.33% (46) of the studied population had coronary artery disease as
the cause of heart failure. In them 60.86% of patients had normal pattern of
PFT, 17.39% had obstructive pattern and 21.73% had restrictive pattern.
38.66% (29) of the studied patients had rheumatic heart disease as the cause
of heart failure. Among them 37.93% had normal pulmonary function test
pattern, while 10.34% had obstructive pattern and 51.72% had restrictive
pattern. From this it is clear that compared to cardiac failure patients with
coronary artery disease, patients with rheumatic heart disease had lower
proportion of patients with normal pulmonary function test pattern. The
prevalence of restrictive pattern of pulmonary function test was more in
those with rheumatic heart disease (51.72%) than those with coronary artery
disease (38.66%).
93
Among the study population 46 patients (61.33) were found to be
hypertensive. In them, 60.86% had normal pattern of pulmonary function
test. 10.86% had obstructive pattern while 28.26% had restrictive pattern.
Out of the studied patients 20 (26.66%) had cardiomegaly on chest
xray. Among them 45% had normal pattern of PFT while 20% had
obstructive pattern and 35% had restrictive pattern.
39 patients (52%) had ejection fraction of more than 50%,. Among
them, 56.41% had normal pulmonary function tests. 5.12% had obstructive
pattern and 38.46% had restrictive pattern. 36 patients (48%) had ejection
fraction less than 50%. Among them, 47.22% had normal pattern of
pulmonary function test while 25% had obstructive pattern and 27.77% had
restrictive pattern. The prevalence of obstructive pattern was more in
patients with left ventricular ejection fraction of less than 50%.
94
CONCLUSION
95
The presence of impaired pulmonary function tests in cardiac failure
patients has been already demonstrated in various studies. This may be due
to various reasons like pulmonary congestion, pulmonary hypertension,
respiratory muscle wasting due to cardiac cachexia and co-existent
respiratory diseases in patients with cardiac failure. More than half of the
cardiac failure patients had normal pulmonary function pattern. In those who
had abnormal pulmonary function pattern, the incidence of restrictive pattern
was more than that of obstructive pattern. The prevalence of restrictive
pattern of pulmonary function test was more in patients with rheumatic heart
disease when compared to patients with coronary artery disease patients for
unknown reason. As the LV ejection fraction of the patients with cardiac
failure decreased there is a higher incidence of obstructive pattern of
pulmonary function test.
96
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97
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ANNEXURE 1
COMMON RESPIRATORY DISEASES BY DIAGNOSTIC METHODS
100
ANNEXURE 2
ALTERATIONS IN VENTILATOR FUNCTIONS
101
ANNEXURE 3
LUNG VOLUMES BY A SPIROGRAPHIC TRACING
102
ANNEXURE 4
NEWYORK HEART ASSOSIATION CLASSIFICATION
103
ANNEXURE 5
ETIOLOGIES OF HEART FAILURE
ANNEXURE 6 – MASTER CHART
104
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ANNEXURE 7
109
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